scholarly journals Endogenous Murine Leukemia Viruses: Relationship to XMRV and Related Sequences Detected in Human DNA Samples

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Oya Cingöz ◽  
John M. Coffin
Keyword(s):  
Sequence Similarity ◽  
Leukemia Virus ◽  
Clinical Samples ◽  
Mouse Virus ◽  
Leukemia Viruses ◽  
Relationship Of ◽  
The Relationship ◽  
Virus Isolates ◽  
Human And Mouse ◽  
Murine Leukemia

Xenotropic-murine-leukemia-virus-related virus (XMRV) was the first gammaretrovirus to be reported in humans. The sequence similarity between XMRV and murine leukemia viruses (MLVs) was consistent with an origin of XMRV from one or more MLVs present as endogenous proviruses in mouse genomes. Here, we review the relationship of the human and mouse virus isolates and discuss the potential complications associated with the detection of MLV-like sequences from clinical samples.

Recent Studies on a Murine Leukemia Virus Grown in Tissue Culture

1967 ◽  
Vol 25 ◽  
pp. 106-107
Author(s):  
L. Z. de Tkaczevski ◽  
E. de Harven ◽  
C. Friend
Keyword(s):  
Tissue Culture ◽  
Solid Tumors ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Supernatant Fluid ◽  
Virus Particles ◽  
Friend Leukemia ◽  
Type C ◽  
Leukemia Viruses ◽  
Murine Leukemia

Despite extensive studies, the correlation between the morphology and pathogenicity of murine leukemia viruses (MLV) has not yet been clarified. The virus particles found in the plasma of leukemic mice belong to 2 distinct groups, 1 or 2% of them being enveloped A particles and the vast majority being of type C. It is generally believed that these 2 types of particles represent different phases in the development of the same virus. Particles of type A have been thought to be an earlier form of type C particles. One of the tissue culture lines established from Friend leukemia solid tumors has provided the material for the present study. The supernatant fluid of the line designated C-1A contains an almost pure population of A particles as illustrated in Figure 1. The ratio is, therefore, the reverse of what is unvariably observed in the plasma of leukemic mice where C particles predominate.

scholarly journals Specificity studies on cytolytic T lymphocytes directed against murine leukemia virus-induced tumors. Analysis of monoclonal cytolytic T lymphocytes.

1982 ◽  
Vol 155 (4) ◽  
pp. 1050-1062 ◽  
Author(s):  
F Plata
Keyword(s):  
T Lymphocytes ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Target Cells ◽  
Cytolytic T Lymphocytes ◽  
Tumor Target ◽  
Induced Tumors ◽  
Definition Of ◽  
Leukemia Viruses ◽  
Murine Leukemia

The specificities of cloned cytolytic T lymphocytes (CTL) were studied for the analysis of CTL populations generated against murine leukemia viruses (MuLV) in H-2 congenic BALB/c (H-2d) and BALB.B (H-2b) mice. In particular, CTL generated in response to tumors induced by Gross MuLV and Friend MuLV were studied; these tumors expressed virus-induced antigens that do not cross-react and that can be distinguished from each other. The systematic study of 92 CTL clones clearly indicated that MuLV-immune CTL were highly heterogeneous with respect to both the intensities of target cell lysis that they mediated and to their specificity of recognition of MuLV-induced tumor target cells. Various categories of CTL clones were identified, ranging from CTL clones tht were tightly H-2 restricted and specific for the immunizing tumor to CTL clones that displayed no discernible patterns of specificity and that attacked a large number of different target cells. In addition, the surface markers of these cloned CTL were defined, and the best conditions for their prolonged maintenance in culture were determined. The present data indicate that future efforts in the definition of target antigens recognized by tumor-specific CTL should be performed with monoclonal lymphocytes.

Generation of infectious Moloney murine leukemia viruses with deletions in the U3 portion of the long terminal repeat

1986 ◽  
Vol 6 (12) ◽  
pp. 4634-4640
Author(s):  
R Hanecak ◽  
S Mittal ◽  
B R Davis ◽  
H Fan
Keyword(s):  
Long Terminal Repeat ◽  
Transient Expression ◽  
Leukemia Virus ◽  
Chloramphenicol Acetyltransferase ◽  
Terminal Repeat ◽  
Tata Box ◽  
Moloney Murine Leukemia Virus ◽  
Chloramphenicol Acetyltransferase Gene ◽  
Leukemia Viruses ◽  
Murine Leukemia

Deletional analysis within the long terminal repeat (LTR) of Moloney murine leukemia virus (M-MuLV) was performed. By molecular cloning, deletions were made in the vicinity of the XbaI site at -150 base pairs (bp) in the U3 region, between the tandemly repeated enhancers and the TATA box. The effects of the deletions on LTR function were measured in two ways. First, deleted LTRs were fused to the bacterial chloramphenicol acetyltransferase gene and used in transient expression assays. Second, infectious M-MuLVs were generated by transfection of M-MuLV proviruses containing the deleted LTRs, and the relative infectivity of the mutant viruses was assessed by XC-syncytial assay. Most of the deleted LTRs examined showed relatively high promoter activity in the transient chloramphenicol acetyltransferase assays, with values ranging from 20 to 50% of the wild-type M-MuLV LTR. Thus, the sequences between the enhancers and the TATA box were not absolutely required for transient expression. However, infectivity of viruses carrying the same deleted LTRs showed more pronounced effects. Deletion of sequences from -195 to -174 bp reduced infectivity 20- to 100-fold. Deletion of sequences within the region from -174 to -122 bp did not affect infectivity, indicating that this region is dispensable. On the other hand, deletion of sequences from -150 to -40 bp reduced infectivity from 5 to 6 logs, although the magnitude of the reduction partly may have reflected threshold envelope protein requirements for positive XC assays. The reduced infectivity did not appear to result from a failure of proviral DNA synthesis or integration by the mutant. Thus, the infectivity measurements identified three functional domains in the region between the enhancers and the TATA box.

scholarly journals Replacement of Murine Leukemia Virus Readthrough Mechanism by Human Immunodeficiency Virus Frameshift Allows Synthesis of Viral Proteins and Virus Replication

2003 ◽  
Vol 77 (5) ◽  
pp. 3345-3350 ◽  
Author(s):  
Marie-Noëlle Brunelle ◽  
Léa Brakier-Gingras ◽  
Guy Lemay
Keyword(s):  
Human Immunodeficiency Virus ◽  
Murine Leukemia Virus ◽  
Stop Codon ◽  
Leukemia Virus ◽  
Viral Proteins ◽  
Immunodeficiency Virus ◽  
Virus Model ◽  
Polyprotein Precursor ◽  
Leukemia Viruses ◽  
Murine Leukemia

ABSTRACT Retroviruses use unusual recoding strategies to synthesize the Gag-Pol polyprotein precursor of viral enzymes. In human immunodeficiency virus, ribosomes translating full-length viral RNA can shift back by 1 nucleotide at a specific site defined by the presence of both a slippery sequence and a downstream stimulatory element made of an extensive secondary structure. This so-called frameshift mechanism could become a target for the development of novel antiviral strategies. A different recoding strategy is used by other retroviruses, such as murine leukemia viruses, to synthesize the Gag-Pol precursor; in this case, a stop codon is suppressed in a readthrough process, again due to the presence of a specific structure adopted by the mRNA. Development of antiframeshift agents will greatly benefit from the availability of a simple animal and virus model. For this purpose, the murine leukemia virus readthrough region was rendered inactive by mutagenesis and the frameshift region of human immunodeficiency virus was inserted to generate a chimeric provirus. This substitution of readthrough by frameshift allows the synthesis of viral proteins, and the chimeric provirus sequence was found to generate infectious viruses. This system could be a most interesting alternative to study ribosomal frameshift in the context of a virus amenable to the use of a simple animal model.

scholarly journals Retroviral Restriction Factors Fv1 and TRIM5α Act Independently and Can Compete for Incoming Virus before Reverse Transcription

2006 ◽  
Vol 80 (5) ◽  
pp. 2100-2105 ◽  
Author(s):  
Luca D. Passerini ◽  
Zuzana Keckesova ◽  
Greg J. Towers
Keyword(s):  
Life Cycle ◽  
Reverse Transcription ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Viral Life Cycle ◽  
Human Cells ◽  
Restriction Factors ◽  
Retroviral Infection ◽  
The Relationship ◽  
Murine Leukemia

ABSTRACT The restriction factors Fv1 and TRIM5α provide dominant blocks to retroviral infection, targeting incoming capsids at a postentry, preintegration step. They both restrict N-tropic murine leukemia virus with similar specificity yet act at different points in the viral life cycle. TRIM5α-restricted virus is usually unable to reverse transcribe, whereas Fv1-restricted virus reverse transcribes normally. Here we investigate the relationship between these two restriction factors by expressing Fv1 alleles in human cells. We demonstrate that Fv1 is able to compete with TRIM5α for virus before reverse transcription. In human cells expressing Fv1b, N-tropic restricted virus becomes less infectious but reverse transcribes more efficiently, indicating competition between the two antiviral molecules and protection of the virus from TRIM5α by Fv1. Our findings suggest that, like TRIM5α, Fv1 interacts with virus before reverse transcription, but the consequences of this interaction are not realized until a later stage of the life cycle. We also demonstrate that Fv1 is functionally independent of TRIM5α when expressed in human cells.

scholarly journals Selection of Optimal Polypurine Tract Region Sequences during Moloney Murine Leukemia Virus Replication

2000 ◽  
Vol 74 (22) ◽  
pp. 10293-10303 ◽  
Author(s):  
Nicole D. Robson ◽  
Alice Telesnitsky
Keyword(s):  
Leukemia Virus ◽  
Moloney Murine Leukemia Virus ◽  
Upstream Sequence ◽  
Wild Type ◽  
The Core ◽  
Polypurine Tract ◽  
Efficient Replication ◽  
Marked Preference ◽  
Leukemia Viruses ◽  
Murine Leukemia

ABSTRACT Retrovirus plus-strand synthesis is primed by a cleavage remnant of the polypurine tract (PPT) region of viral RNA. In this study, we tested replication properties for Moloney murine leukemia viruses with targeted mutations in the PPT and in conserved sequences upstream, as well as for pools of mutants with randomized sequences in these regions. The importance of maintaining some purine residues within the PPT was indicated both by examining the evolution of random PPT pools and from the replication properties of targeted mutants. Although many different PPT sequences could support efficient replication and one mutant that contained two differences in the core PPT was found to replicate as well as the wild type, some sequences in the core PPT clearly conferred advantages over others. Contributions of sequences upstream of the core PPT were examined with deletion mutants. A conserved T-stretch within the upstream sequence was examined in detail and found to be unimportant to helper functions. Evolution of virus pools containing randomized T-stretch sequences demonstrated marked preference for the wild-type sequence in six of its eight positions. These findings demonstrate that maintenance of the T-rich element is more important to viral replication than is maintenance of the core PPT.

scholarly journals Phylogenetic Relationship of the Complete Rauscher Murine Leukemia Virus Genome with Other Murine Leukemia Virus Genomes

Virology ◽  
1997 ◽  
Vol 238 (1) ◽  
pp. 64-67 ◽  
Author(s):  
Anis H Khimani ◽  
Michael Lim ◽  
Thomas G Graf ◽  
Temple F Smith ◽  
Ruth M Ruprecht
Keyword(s):  
Phylogenetic Relationship ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Virus Genome ◽  
Virus Genomes ◽  
Relationship Of ◽  
Murine Leukemia
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